ArticleNPJ Parkinson's disease2026
Glucose-responsive AMPK-TET2-5hmc oscillation links metabolic stress to circadian transcription and Parkinson's disease relevance.
Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Circadian disruption and metabolic stress are implicated in Parkinson's disease (PD), but the epigenetic mechanisms linking nutrient fluctuations to circadian regulation remain poorly understood. Here, we combined genome-wide 5-hydroxymethylcytosine (5hmC) profiling, CRISPR-based genetic perturbations, and circadian models to investigate how glucose availability shapes epigenetic dynamics and circadian transcription. We found that low glucose activates AMP-activated protein kinase (AMPK), upregulating TET2 transcription and increasing global 5hmC remodeling. These effects are reversible upon glucose restoration and are abolished by AMPK deficiency, establishing AMPK as a key mediator of metabolic control over TET2. Notably, Tet2 exhibits intrinsic circadian rhythmicity and is temporally coupled with clock-associated gene expression. Disruption of TET2 impairs glucose-responsive 5hmC dynamics and alters circadian transcriptional outputs. Together, our findings define a glucose-responsive AMPK-TET2-5hmC axis that links metabolic state to epigenetic and circadian regulation. This work provides a mechanistic framework for understanding how metabolic dysfunction may contribute to circadian abnormalities in Parkinson's disease.
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